IFNB1 (Interferon Beta 1)

The reprogrammed macrophages induced apoptosis and cell cycle arrest (G0/G1 and G2/M phases) in 4T1 breast cancer cells. In conclusion, the PLGA-CM1-CDN-R848 NPs formulation represents a promising strategy for breast cancer immunotherapy by targeting M2 TAMs within the TME and reprogramming them toward the M1 phenotype.

We validated this method using DNA samples from peripheral blood and buccal swabs from 17 healthy human volunteers, as well as umbilical cord blood from 9 healthy newborn babies, demonstrating its high linearity and reproducibility. Our findings indicate that this improved qPCR technique provides a rapid, cost-effective, and accurate means of measuring absolute telomere length, thereby facilitating large-scale studies and enhancing clinical diagnostics related to telomere biology.

The strong correlation between UNC93B1 overexpression and adverse clinical outcomes underscores its potential as a dual diagnostic biomarker and therapeutic target. This work not only provides a mechanistic foundation for novel precision immunotherapies in PDAC but also establishes a robust methodological paradigm for multi-omics-driven discovery in oncology.

P=N/A, N=77, Completed, University Hospital, Rouen | Recruiting --> Completed

P=N/A, N=1214, Recruiting, Novartis Pharmaceuticals | Active, not recruiting --> Recruiting | N=564 --> 1214 | Trial completion date: Dec 2026 --> May 2029 | Trial primary completion date: Dec 2026 --> May 2029

In a 4T1 residual-tumor model established by partial tumor resection, a staged regimen consisting of cPAG-assisted irreversible electroporation followed by cPAG-mediated photothermal therapy showed the strongest suppression of local tumor regrowth among tested groups, with maintained body weight during the study window. Overall, cPAG provides a modular nano-in-micro depot strategy to integrate multiple local treatments for postoperative control of TNBC tumor.

Thus, we discovered a novel pathogen-related GPS gene family in the human genome, and its pericentromeric transcription-regulatory network. This discovery will help to understand the role of GPS pericentromeric transcription in the biology, immunotherapy, and host-pathogen relationships of cancers in the future.

In vivo, co‑treatment enhanced IFN‑β induction, increased CD8⁺ T‑cell infiltration and reduced tumor burden relative to monotherapies, whereas efficacy was not observed in athymic nude mice, supporting T‑cell dependence. Together, these data provide preclinical evidence that a rational oncolytic virus and STING combination can amplify antitumor immunity without overtly compromising viral persistence.

In contrast, the activation or expression of the two other IFN transcription factors, the NF-κB subunit RelA and the AP-1 subunit ATF2, correlated with IFN-β induction. Our results suggest that during viral infection, activation of IRF3 does not automatically result in IFN responses at the level of individual cells, but that other factors, such as NF-κB and AP-1, are limiting for type I IFN induction.

Transcriptomic analysis further reveals that CDN@VLP promotes cDC1 recruitment into tumors by enhancing the secretion of key chemokines (XCL1, CCL4, and CCL5), suggesting an additional mechanism of action. By mimicking viral tropism, the CDN@VLP platform establishes a paradigm for precision STING activation, overcoming the trade-off between potency and specificity in cDC1-targeted immunotherapy.

Using orthotopic and metastatic BCa tumors, we demonstrated this nanoplatform could suppress the proliferation of BCa cells via siRNA-mediated Carm1 silencing and down-regulate programmed death-ligand 1 (PD-L1) expression via metformin-mediated ubiquitin-proteasome degradation. More importantly, due to the important role of oncogene Carm1 in repairing damaged double stand DNA (dsDNA), Carm1 silencing could specifically enhance the accumulation of damaged dsDNA and cytosolic release of dsDNA fragments to precisely activate the cGAS-STING pathway in BCa cells, which could thus promote their expression and secretion of interferon-β (IFN-β) to induce a significant inhibition of BCa tumor growth via leveraging both the innate and adaptive immunity.

Our results indicate a promising and efficient strategy for the encapsulation and targeted delivery of venetoclax using HFn nanoparticles for AML patients. This delivery system can support co-delivery of various drugs and combination therapy of tumor cells.